Cardiovascular Complications of Diabetes Mellitus: Mechanisms and Novel Treatment Approaches

Laura Vero^*
*Correspondence: Laura Vero, Department of Cardiology, University of Oulu, Pentti Kaiteran katu 1, 90570 Oulu, Finland, Email:

Keywords

Coronary heart disease • Cardiovascular complications • Diabetes mellitus

Introduction

Diabetes mellitus is a global health epidemic, affecting approximately 463 million people worldwide, and its prevalence is expected to rise in the coming years. Cardiovascular disease is the leading cause of morbidity and mortality among individuals with diabetes. People with diabetes have a two- to four-fold increased risk of developing CVD compared to those without diabetes. The mechanisms linking diabetes to CVD are complex and multifaceted, involving several interconnected pathways. This article aims to elucidate the mechanisms responsible for the cardiovascular complications of diabetes and explore novel treatment approaches to mitigate these risks. Chronic hyperglycemia, a hallmark of diabetes, contributes significantly to the development of cardiovascular complications [1-3].

Elevated blood glucose levels lead to the formation of advanced glycation end-products, oxidative stress, endothelial dysfunction, and inflammation. These processes collectively promote atherosclerosis, myocardial infarction, and stroke. Insulin resistance is a metabolic condition in which the body's cells do not respond effectively to the hormone insulin. Insulin is produced by the pancreas and plays a crucial role in regulating blood sugar (glucose) levels. When you eat carbohydrates, your body breaks them down into glucose, which enters the bloodstream. Insulin helps transport this glucose from the bloodstream into cells, where it can be used for energy or stored for future use. In a healthy individual, cells respond to insulin by allowing glucose to enter and be used for energy. However, in people with insulin resistance, the cells become less responsive to insulin's signals.

Glucose levels in the bloodstream remain elevated, leading to hyperglycemia (high blood sugar). The pancreas produces more insulin to compensate for the reduced effectiveness, leading to higher levels of insulin in the blood (hyperinsulinemia). The body may store excess glucose as fat, contributing to weight gain and obesity. Over time, the pancreas may become exhausted and unable to produce enough insulin to keep blood sugar levels in check, leading to type 2 diabetes. Insulin resistance is a key factor in the development of type 2 diabetes, a chronic condition characterized by high blood sugar levels.

Literature Review

Insulin resistance can contribute to weight gain, and excess body fat, especially around the abdomen, can worsen insulin resistance. Insulin resistance is linked to hypertension (high blood pressure). It can lead to elevated levels of triglycerides and low-density lipoprotein cholesterol, increasing the risk of cardiovascular disease. Many women with PCOS have insulin resistance, which can lead to irregular menstrual cycles, infertility, and other symptoms. Insulin resistance is a risk factor for the development of fatty liver disease.

Several factors contribute to the development of insulin resistance, including genetics, obesity, physical inactivity, poor diet (especially one high in processed sugars and refined carbohydrates), and certain medical conditions. Managing insulin resistance often involves lifestyle changes, such as losing weight, increasing physical activity, and adopting a balanced diet. In some cases, medication may be prescribed to help improve insulin sensitivity. Early detection and management of insulin resistance are important to prevent or delay the onset of type 2 diabetes and reduce the risk of associated health complications. If you suspect you may have insulin resistance or are concerned about your blood sugar levels, it's essential to consult a healthcare professional for evaluation and guidance. Chronic low-grade inflammation and oxidative stress play pivotal roles in the pathogenesis of diabetic cardiovascular complications. Inflammatory cytokines and reactive oxygen species damage vascular endothelium, initiate atherogenesis, and promote plaque instability [4,5].

Dyslipidemia refers to an abnormal level of lipids (fats) in the blood, including cholesterol and triglycerides. It is a common metabolic disorder that can increase the risk of cardiovascular diseases, such as heart disease and stroke. Elevated levels of low-density lipoprotein cholesterol, often referred to as "bad" cholesterol, are a common feature of dyslipidemia. High LDL-C levels are associated with an increased risk of atherosclerosis, where fatty deposits accumulate in the arteries, leading to narrowing and blockages.

Discussion

HDL-C is often called "good" cholesterol because it helps remove excess cholesterol from the bloodstream and transport it to the liver for disposal. Low levels of HDL-C are a risk factor for heart disease. Triglycerides are another type of fat in the blood, and elevated triglyceride levels can be associated with dyslipidemia. High triglycerides can also contribute to atherosclerosis and increase the risk of cardiovascular problems. Dyslipidemia can be caused by various factors, including genetics, diet, lifestyle, and underlying medical conditions. A diet high in saturated fats, transfats, and cholesterol can lead to elevated LDL-C and triglyceride levels. Lack of physical activity can contribute to dyslipidemia and other cardiovascular risk factors.

Being overweight or obese is often associated with dyslipidemia. Some people may have a genetic predisposition to dyslipidemia, leading to higher cholesterol and triglyceride levels. People with diabetes are at an increased risk of dyslipidemia. Dyslipidemia is typically diagnosed through blood tests that measure lipid levels, including total cholesterol, LDL-C, HDL-C, and triglycerides. Treatment for dyslipidemia aims to reduce the risk of cardiovascular events and may involve lifestyle changes and medications, such as statins or other lipid-lowering drugs. Common lifestyle modifications include adopting a heart-healthy diet, increasing physical activity, losing weight if necessary, quitting smoking, and limiting alcohol intake.

It's essential to manage dyslipidemia effectively because it is a significant modifiable risk factor for heart disease and stroke. Individuals with dyslipidemia often work closely with healthcare professionals to develop a personalized treatment plan to improve their lipid profile and reduce the risk of cardiovascular complications. Regular monitoring and adherence to treatment recommendations are crucial for managing dyslipidemia effectively. Glycemic control remains a cornerstone in diabetes management to reduce the risk of CVD. Novel glucose-lowering agents such as SGLT-2 inhibitors and GLP-1 receptor agonists have demonstrated cardiovascular benefits beyond glycemic control [6].

Thiazolidinediones, which improve insulin sensitivity, have shown potential in reducing CVD risk in certain populations. However, their side effects need to be carefully considered. Emerging therapies targeting inflammation and oxidative stress, including specific anti-inflammatory agents and antioxidants, hold promise in preventing or ameliorating diabetic cardiovascular complications. Tailoring treatment strategies based on individual patient profiles, including genetic, metabolic, and lifestyle factors, may enhance outcomes and reduce CVD risk in diabetes. Promoting healthy lifestyle choices, such as regular physical activity, a balanced diet, and smoking cessation, remains fundamental in managing diabetes and reducing CVD risk.

Conclusion

Cardiovascular complications represent a significant burden in individuals with diabetes mellitus. Understanding the intricate mechanisms linking diabetes to CVD is essential for developing effective prevention and treatment strategies. Novel therapeutic approaches, including glucose-lowering agents with cardiovascular benefits, insulin sensitizers, anti-inflammatory agents, antioxidants, personalized medicine, and lifestyle interventions, offer hope for improving cardiovascular outcomes in this high-risk population. A comprehensive, multidisciplinary approach is essential to address the complex interplay of factors contributing to cardiovascular complications in diabetes and ultimately reduce the associated morbidity and mortality.

Acknowledgement

None.

Conflict of Interest

Authors declare no conflict of interest.

References

1. Qi, Lu, Layla Parast, Tianxi Cai and Christine Powers, et al. "Genetic susceptibility to coronary heart disease in type 2 diabetes: 3 independent studies." J Am Coll Cardiol 58 (2011): 2675-2682.

Google Scholar, Crossref, Indexed at

2. Marston, Nicholas A., Frederick K. Kamanu, Francesco Nordio and Yared Gurmu, et al. "Predicting benefit from evolocumab therapy in patients with atherosclerotic disease using a genetic risk score: Results from the fourier trial." Circulation 141 (2020): 616-623.

Google Scholar, Crossref, Indexed at

3. Heald, Adrian H., Mike Stedman, Mark Davies and Mark Livingston, et al. "Estimating life years lost to diabetes: Outcomes from analysis of National Diabetes Audit and Office of National Statistics data." Cardiovasc Endocrinol Metab 9 (2020): 183.

Google Scholar, Crossref, Indexed at

4. Johansson, Mats, Anna Ehnvall, Peter Friberg and Anna Myredal. "Arterial baroreflex dysfunction in major depressive disorder." J Clin Auton Res 20 (2010): 235-240.

Google Scholar, Crossref, Indexed at

5. Tamler, Ronald. "Diabetes, obesity, and erectile dysfunction." J Gend Med 6 (2009): 4-16.

Google Scholar, Crossref, Indexed at

6. Cui, Xiaoming, Jing Zhou, Zongshi Qin and Zhishun Liu. "Acupuncture for erectile dysfunction: A systematic review." J BioMed Res Int 2016 (2016).

Google Scholar, Crossref, Indexed at